Ischemia changes the coexpression of somatostatin and neuropeptide Y in hippocampal interneurons
Ischemia changes the coexpression of somatostatin and neuropeptide Y in hippocampal interneurons
复制标题
DOI：
10.1007/pl00005712
复制
发表时间：
1997-07-01
影响因子：
2
通讯作者：
Johansen, FF
中科院分区：
文献类型：
--
作者：
Bering, R;Draguhn, A;Johansen, FF
短暂性脑缺血可导致大鼠海马区CA1区锥体细胞广泛死亡和齿状门区中间神经元选择性丢失。许多海马区中间神经元可根据其生长抑素(SS)和/或神经肽Y(NPY)的含量进行分类。大鼠脑缺血后，大部分NPY免疫反应在海马区永久性丧失。此外，在缺血后16天内，齿状脑门SS中间神经元死亡，而CA1中间神经元存活，其SS mRNA和多肽的表达恢复到缺血前水平。我们解决了以下问题：(1)NPY的丢失是否涉及缺血前同时表达SS和NPY的存活的CA1中间神经元的特异性下调？(2)从缺血前SS和NPY的共同表达能否识别门区死亡的中间神经元的亚群？我们用原位杂交和免疫细胞化学相结合的方法研究了SS基因和NPY多肽的共表达。取缺血后2~16d的对照组和海马区切片，计数含有一个或两个标志物的细胞数。在CA1区，仅含NPY的神经元数量减少，同时表达NPY和SS的神经元数量减少，而仅含SS的神经元数量在缺血16d后增加。我们的结论是，在缺血前共表达SS和NPY的神经元增加了缺血后仅含SS的神经元的数量，这是因为在共表达群体中NPY的表达被选择性地下调。在门区，我们证明了表达SS和NPY或两者都表达的神经元存活和缺血细胞死亡，这表明不能明确地从SS和NPY在缺血前的共存来识别因缺血而死亡的门区中间神经元。
Transient cerebral ischemia causes extensive cell death in hippocampal CA1 pyramidal cells and selective loss of interneurons in the dentate hilus. Many hippocampal interneurons can be classified by their contents of somatostatin (SS) and/or neuropeptide Y (NPY). Following ischemia in the rat, most of the NPY immunoreactivity is permanently lost in hippocampus. Furthermore, SS interneurons in the dentate hilus die, whereas CA1 interneurons survive and their expression of SS mRNA and peptide returns to preischemic levels within 16 days after ischemia. We have addressed the following questions: (1) Does the loss of NPY involve a specific downregulation in surviving CA1 interneurons that preischemically expressed both SS and NPY? (2) Can the subpopulation of dying interneurons in hilus be identified from their pre ischemic coexpression of SS and NPY? We investigated the coexpression of SS mRNA and NPY peptide using combined in situ hybridization and immunocytochemistry. Cells containing one or both markers were counted in control sections and sections taken 2-16 days after ischemia from the hippocampal formation. In CA1, a decrease in the number of neurons containing NPY alone as well as a decrease in the number of neurons coexpressing NPY and SS was observed, whereas the number of neurons containing SS alone increased 16 days after ischemia. We conclude that neurons coexpressing SS and NPY before ischemia added to the number of neurons containing SS alone after ischemia, because NPY expression was selectively downregulated in the coexpressing population. In hilus, we demonstrated both survival and ischemic cell death of neurons expressing either SS, NPY or both, indicating that hilar interneurons dying from ischemia cannot unequivocally be identified from their preischemic colocalization of SS and NPY.